Rutin is a valuable traditional Chinese medicine known for its anti-inflammatory and anticancer effects. It has been shown to be effective in treating various inflammation-associated diseases. Here, we investigated the influence of rutin on acute pancreatitis and tumorigenesis. Using C57BL/6J mice and Kras mutant transgenic mice, we induced pancreatitis and acinar regeneration models. Pancreatic malondialdehyde (MDA), superoxide dismutase (SOD) activity and reduced glutathione (GSH) contents were measured for oxidative stress. Histological staining and a pancreatic acinar 3D culture model were used to clarify the influence of rutin on ADM in vivo and in vitro. Western blotting was adopted to detect ADM markers amylase and CK19. We found that rutin ameliorated inflammatory injury to the pancreas in both caerulein- and arginine-induced AP. Then, we revealed that the anti-damage effect of rutin may be due to its inhibition of oxidative stress. In addition, an acinar 3D culture model showed that rutin inhibited the formation of ADM by activating AMPK in acinar cells. Finally, the activation of AMPK is believed to be a potential mechanism by which rutin exerts inhibitory effects on Kras-driven tumorigenesis. Rutin inhibited AP-induced pancreatic injury and oncogenic Kras-driven tumorigenesis by inhibiting ADM.

Pancreatic ductal adenocarcinoma (PDAC) is recognized as one of the most lethal malignancies, characterized by late-stage diagnosis and limited therapeutic options. Risk stratification has traditionally been performed using epidemiological studies and genetic analyses, through which key risk factors, including smoking, diabetes, chronic pancreatitis, and inherited predispositions, have been identified. However, the multifactorial nature of PDAC has often been insufficiently addressed by these methods, leading to limited precision in individualized risk assessments. Advances in artificial intelligence (AI) have been proposed as a transformative approach, allowing the integration of diverse datasets-spanning genetic, clinical, lifestyle, and imaging data into dynamic models capable of uncovering novel interactions and risk profiles. In this review, the evolution of PDAC risk stratification is explored, with classical epidemiological frameworks compared to AI-driven methodologies. Genetic insights, including genome-wide association studies and polygenic risk scores, are discussed, alongside AI models such as machine learning, radiomics, and deep learning. Strengths and limitations of these approaches are evaluated, with challenges in clinical translation, such as data scarcity, model interpretability, and external validation, addressed. Finally, future directions are proposed for combining classical and AI-driven methodologies to develop scalable, personalized predictive tools for PDAC, with the goal of improving early detection and patient outcomes.

Alcohol significantly contributes to pancreatitis, causing high global mortality and health burden. This study examines trends in alcohol-attributable pancreatitis (AAP) from 1990 to 2021 using Global Burden of Disease (GBD) 2021 data, focusing on demographic, temporal, and regional variations to inform policymaking.

AAP-related deaths and disability-adjusted life years (DALYs) were analyzed across 204 countries from 1990 to 2021, stratified by Sociodemographic Index (SDI), gender, and age groups. An age-period-cohort model assessed age-standardized DALY rates (ASDR), and decomposition analysis quantified impacts of population growth, aging, and epidemiological changes.

AAP-related DALYs rose from 401,700 in 1990 to 699,300 in 2021, though ASDR and ASMR showed declines globally. Burden increased notably in low and lower-middle SDI regions, especially among those under 40, while high SDI regions achieved better control. Males faced a disproportionately high burden due to alcohol consumption patterns, although some regions saw rising female burdens. Low-SDI areas suffered from limited healthcare, increasing alcohol use, and weak policies, with younger populations contributing significantly to rising burdens. Projections estimate 1.146 million DALYs annually by 2050, with males comprising over 90%. A GBD-AAP visualization platform was developed to present burden data and trends.

AAP exhibits significant regional and gender disparities. Targeted measures, including alcohol regulation, resource allocation, and public health education, are critical in low-SDI regions and among young males to mitigate AAP burden. The GBD-AAP platform offers valuable tool for targeted interventions.

Plasma metabolite levels in patients with pancreatic cancer (PC) have changed, but the relationship between the altered plasma metabolites and the risk for PC occurrence is not fully clear, as well as the predictive value of the specific metabolites.

In this study, we obtained the metabolomics data of 243,145 people from the UK Biobank. An extreme gradient boosting (XGBoost) model, least absolute shrinkage and selection operator (Lasso) regression, and covariate-adjusted Cox proportional hazard regression models were used to evaluate the relationship between metabolites and PC risk. We also evaluated conventional risks, metabolites, and combination models for PC risk by comparing the area under the receiver operating characteristic curve (AUC).

The average follow-up time was 13.8 (± 2.1) years; 1,026 of 243,145 participants developed PC. Fourteen metabolites were significantly associated with PC, including glucose-related metabolites, lipids, lipoproteins, and amino acids. Increased PC risk was associated with citrate, glucose, and the percentage of triglycerides to total lipids in intermediate-density lipoprotein or small low-density lipoprotein. Glycine, histidine, cholesterol, and cholesterol ester subclasses were associated with lower PC risk. Predicting PC risk improved when the newly identified metabolites were added to conventional PC risk factors (AUC: 0.705 vs 0.711, p = 0.037). The Kaplan-Meier cumulative incidence curves showed that these metabolites were good predictors of PC risk (all log-rank p < 0.05).

We identified novel metabolites that were significantly associated with the occurrence of PC, which may aid in the early diagnosis of PC.

There is a well-established link between the severity of hypertriglyceridaemia and acute pancreatitis and long-term triglyceride-lowering therapies known to prevent episodes of acute pancreatitis. Therefore, it has been assumed, without firm evidence, that rapid lowering of plasma triglycerides would be an effective strategy for reducing the clinical severity of acute pancreatitis and improving health outcomes. Therapies, such as intravenous heparin, intravenous insulin in normoglycaemic individuals (with glucose to prevent hypoglycaemia), and plasmapheresis, continue to be widely used as therapeutic interventions to rapidly reduce serum triglyceride concentration. These therapies are all associated with a risk of adverse reactions, require increased resources, and increase health-care costs. Randomised controlled clinical trials of these therapies have generally shown more rapid reductions in plasma triglycerides than conventional supportive care with the patient made nil by mouth. However, these three therapies alone or in combination, have failed to show effectiveness in improving substantial health benefit outcome measures. While we recognise the theoretical basis for rapidly reducing plasma triglycerides in hypertriglyceridaemia-induced pancreatitis-based on our review of studies using heparin, insulin, plasmapheresis, or a combination of these-these strategies overall do not reduce complications associated with acute pancreatitis or the rapidity of disease resolution. Therefore, we do not advocate the use of triglyceride-lowering therapies at this time, pending more convincing evidence.

Neutrophils can undergo transcriptional and epigenetic reprogramming in disease, thus causing inflammation or modulating tissue repair and fibrosis. A thorough understanding of the neutrophil subpopulation composition and their polarization processes in acute pancreatitis (AP) is essential to open up design of treatments tailored to individual patients. Herein, this study distinct subgroups and two differentiation pathways associated with N1 and N2 polarization during AP by single-cell sequencing. Inspired by this, a hollow manganese dioxide (HMnO2)-based nanoreactor (Pyp@APHM) conjugated with neutrophil-binding Ly-6G antibody and loaded with porphyrin is developed for targeted and in situ modulation of neutrophil polarization. Pyp@APHM can enrich the AP site by hitchhiking on neutrophils and then degrade in response to a weakly acidic environment to simultaneously release manganese ions and porphyrin ligands, enabling in situ synthesis of manganese porphyrin antioxidants. Leveraging this strategy, Pyp@APHM can effectively eliminate reactive oxygen species (ROS) and broadly inhibit both N1 and N2 polarization, as well as enhance tissue oxygenation by generating O2, thereby further mitigating pancreatic inflammation. This study provides a comprehensive single-cell atlas of neutrophils in AP and proposes an innovative hitchhiking therapeutic strategy for AP by restricting ROS in neutrophils.

Pancreatic cancer (PC), particularly pancreatic ductal adenocarcinoma (PDAC), is a significant global health issue with high mortality rates. PDAC, though only 3 % of cancer diagnoses, causes 7 % of cancer deaths due to its severity and asymptomatic early stages. Risk factors include lifestyle choices, environmental exposures, and genetic predispositions. Conditions like new-onset type 2 diabetes and chronic pancreatitis also contribute significantly. Modifiable risk factors include smoking, alcohol consumption, non-alcoholic fatty pancreatic disease (NAFPD), and obesity. Smoking and heavy alcohol consumption increase PC risk, while NAFPD and obesity, particularly central adiposity, contribute through chronic inflammation and insulin resistance. Refined sugar and sugar-sweetened beverages (SSBs) are also linked to increased PC risk, especially among younger individuals. Hormonal treatments and medications like statins, aspirin, and metformin have mixed results on PC risk, with some showing protective effects. The gut microbiome influences PC through the gut-pancreas axis, with disruptions leading to inflammation and carcinogenesis. Exposure to toxic substances, including heavy metals and chemicals, is associated with increased PC risk. Glycome changes, such as abnormal glycosylation patterns, are significant in PDAC development and offer potential for early diagnosis. Interactions between environmental and genetic factors are crucial in PDAC susceptibility. Genome-wide association studies (GWAS) have identified several single nucleotide polymorphisms (SNPs) linked to PDAC, but gene-environment interactions remain largely unexplored. Future research should focus on polygenic risk scores (PRS) and large-scale studies to better understand these interactions and their impact on PDAC risk.

This study mainly reports a case of a middle-aged man who was admitted to the hospital due to sudden upper abdominal pain after several hours. After being given the painkiller compound diclofenac sodium in the outpatient clinic, the patient suffered from systemic itching, redness, and rash. Acute pancreatitis was diagnosed after admission. During the treatment, the patient had allergic reactions to multiple drugs. This case is rare. In this case, case reports are used for improving the understanding of multi-drug allergies by clinical pharmacists and clinicians, which offers certain reference for dealing with the safety and effectiveness of medication in patients undergoing multi-drug allergies.

Background: PC has become a significant global health challenge, with incidence and mortality rates rising over the past three decades. While traditionally associated with aging, recent data indicate an increasing burden among younger populations. This study aims to analyze global trends in PC incidence and mortality and to identify key contributing factors, particularly modifiable risk factors such as obesity, diabetes, and smoking. Methods: Using data from the Global Burden of Disease Study (GBD) 2021, population-based cancer registries globally and nationally, systematic reviews and analysis trends in PC incidence, mortality and survival were analyzed. To assess epidemiological shifts, we utilized previously published annual percentage change (AAPC) values stratified by region, age group, and sex, as reported in the cited literature. Additionally, the influence of modifiable risk factors was evaluated to determine their contribution to rising incidence rates. Results: Between 1990 and 2021, the global incidence of PC increased by 8.9%, from 5.47 to 5.96 per 100,000, with the highest rates observed in high-Sociodemographic-Index (SDI) regions (10.00 per 100,000) and the lowest in low-SDI regions (1.59 per 100,000). Significant increases in incidence were noted in several countries, particularly among men in Iceland (AAPC 8.85) and women in Malta (AAPC 6.04). Early-onset PC is becoming more prevalent, especially among younger women. Modifiable risk factors, including obesity, diabetes, and smoking, play a critical role, with excess body weight contributing to 17.9% of PC cases and smoking to 13.9% in the United States (U.S.). Conclusions: The rising burden of PC, particularly among younger populations, highlights the need for targeted prevention strategies, early detection efforts, and further research into the underlying mechanisms driving these trends. Addressing modifiable risk factors could be key to mitigating the increasing incidence of this highly lethal cancer.

Hyperstimulation with the secretagogue cerulein is a commonly used experimental model to study acute, recurrent acute and chronic pancreatitis in mice. Earlier studies showed that inbred mouse strains had different susceptibility to cerulein-induced pancreatitis. Here, we confirm and extend these findings by characterizing the severity of acute and recurrent acute pancreatitis in the C57BL/6N and FVB/N strains. When acute pancreatitis was induced with repeated cerulein injections, FVB/N mice had more severe pancreatic edema, higher plasma amylase levels, increased inflammatory cell infiltration, and more extensive acinar cell necrosis relative to the C57BL/6N strain. Cerulein elicited higher and more sustained trypsin activity in FVB/N mice relative to C57BL/6N animals, which was likely due to the lower expression of the SPINK1 trypsin inhibitor and the trypsinogen-degrading lysosomal protease cathepsin L. In C57BL/6N mice, we previously showed that pancreatitis responses were more severe during a second attack compared with the initial, sentinel episode. In FVB/N mice, we now found that the second episode was associated with lower pancreas edema and plasma amylase but higher inflammatory cell infiltration than the first attack. The observations reinforce the notion that inbred mouse strains exhibit differences in their pathological responses during acute and recurrent acute pancreatitis.

Immune checkpoint inhibitor (ICI) have shown promising results against a variety of solid tumors across clinical trials. However, ICI monotherapy is often ineffective in patients with non-immunogenic tumors that exhibit high level of immunosuppression and low level of tumor infiltrating lymphocytes. To address these limitations, we have investigated a combination of ICIs [anti-PD-1 antibody (αPD-1), anti-PD-L1 antibody (αPD-L1), or anti-CTLA-4 antibody (αCTLA-4)] with several different immune stimulatory oncolytic adenoviruses (Ads) expressing different combinations of antitumor cytokines or immune modulatory factors [e.g., (1) interleukin (IL)-12 and granulocyte-macrophage colony-stimulating factor (GM-CSF; RdB/IL12/GMCSF), (2) IL-12 and short hairpin ribonucleic acid (shRNA) targeting vascular endothelial growth factor (RdB/IL12/shVEGF), (3) IL-12 and decorin (RdB/IL12/DCN), (4) GM-CSF, and thymidine kinase (RdB/IL12/GMCSF-TK), or (5) IL-12, GM-CSF, and relaxin (RdB/IL12/GMCSF-RLX)] to overcome tumor-induced immunosuppression. Through comparative evaluation of combination therapy regimens, our findings have identified αPD-1 as the optimal ICI candidate to synergize with different oncolytic Ads to induce potent antitumor immune response against poorly immunological solid tumors.

This study analyzes temporal trends of pancreatitis from 1990 to 2021 across 21 regions and 204 countries based on the Global Burden of Disease (GBD) database to inform prevention and treatment strategies.

Incidence, death, prevalence, and DALYs estimates for pancreatitis were derived from the GBD 2021, categorized by age, sex, and geographical location for the period 1990-2021. Mortality estimates were generated using the cause of death ensemble model.

The global age-standardized incidence and deaths of pancreatitis increased 1.59-fold and 1.79-fold from 1990 to 2021, respectively. The percentage change in global age-standardized incidence and death rate were -12.8% (-14.7% to -10.7%) and -14.1% (-24.5% to -1.1%). DALYs increased from 2.58 million in 1990 to 4.10 million in 2021. The incidence rates in 2021 ranged from 16.63 per 100 000 in Tropical Latin America, the lowest globally, to 99.35 per 100 000 in Eastern Europe, the highest. Greenland reported the highest country-specific incidence at 115.21 per 100 000, whereas Mozambique had the lowest at 0.81 per 100 000. The incidence and death rates were higher in males, with ratios of 1.27:1 and 1.94:1, respectively. The main contributors to pancreatitis was alcohol use.

Pancreatitis continues to exhibit a heavy burden on a global scale, particularly in Eastern Europe. Therefore, efficient prevention and control strategies targeting alcohol consumption are imperative in order to alleviate the substantial burden.

Isotonic crystalloids are recommended as the first choice for fluid therapy in acute pancreatitis (AP), with normal saline (NS) and lactate Ringer's (LR) used most often. Evidence based recommendations on the type of fluid are conflicting and generally come from small single-center randomized controlled trials (RCTs). We therefore conducted a systematic review and meta-analysis to compare the effect of balanced solutions (BS) versus NS on patient-centered clinical outcomes in AP.

From four databases searched up to October 2024, we included only RCTs of adult patients with AP that compared the use of BS (including LR, acetate Ringer's, etc.) with NS. The primary outcome was the disease advances from AP to moderately severe and severe AP (MSAP/SAP). Trial sequential analyses (TSA) were conducted to control for type-I and type-II errors and Grading of Recommendations Assessment, Development, and Evaluation (GRADE) was used to assess the quality of evidence.

Six RCTs were identified and included, involving 260 patients treated with BS and 298 patients with NS. Patients who received the BS had less MSAP/SAP [odds ratio (OR) = 0.50, 95 % confidence interval (CI): 0.29 to 0.85, P = 0.01, I2 = 0 %; 5 studies, 299 patients], reduced need of ICU admission (OR = 0.60, 95 % CI: 0.39 to 0.93, P = 0.02, I2 = 0 %; 5 studies, 507 patients) and shorter length of hospital stay [mean difference (MD) = -0.88, 95 % CI:1.48 to -0.28, P = 0.004, I2 = 0 %; 6 studies, 558 patients; confirmed by TSA with high certainty] compared with those who received NS. The evidence for most of the clinical outcomes was rated as moderate to low due to the risk of bias, imprecision and inconsistency.

BS, compared with NS, was associated with improved clinical outcomes in patients with AP. However, given the moderate to low quality of evidence for most of the outcomes assessed, further trials are warranted.

Pathological examination of lymph node metastasis (LNM) is crucial for treating pancreatic ductal adenocarcinoma (PDAC). Although the tumour stroma is correlated with prognosis in multiple solid tumors, its role in detecting LNM in PDAC is unclear. Thus, this study aimed to investigate the relationship of tumor-stroma ratio (TSR) with LNM, survival and mutational profile in PDAC.

In this multicenter retrospective study, we examined molecular and clinicopathologic features of 737 PDAC patients from 5 independent cohorts, including surgically resected and endoscopic ultrasound fine-needle aspiration (EUS-FNA) biopsy specimens. TSR was evaluated on hematoxylin and eosin-stained slides and classified as stroma-low (<50% stroma) or stroma-high (≥50% stroma).

Compared to TSR-high cases, TSR-low cases were significantly associated with LNM (P < 0.001). TSR could accurately distinguish patients with and without LNM with an area under curve (AUC) of 0.749, with the sensitivity and specificity of 76.5% and 71.6%, respectively. This accuracy of TSR for identifying LNM was further increased by adding other factors including PD-L1 expression or pretreatment serum CA19-9 levels. TSR showed similar levels of accuracy in analysis of resected tumor specimens and EUS-FNA biopsies. Moreover, we found that TSR could also identify residual nodal involvement after neoadjuvant therapy (NAT) using pretreatment EUS-FNA biopsy samples. Heterogeneous genetic alterations were observed between TSR-low and TSR-high subgroups. TSR was identified as an independent predictor of LNM and worse disease-free survival. Major findings were all reproducible in validation, EUS-FNA biopsy, and pre-treatment NAT EUS-FNA biopsy cohorts.

TSR served as a robust and reproducible biomarker that identifies patients at risk for LNM. TSR might be used to select treatment and management strategies for PDAC patients.

Although acute pancreatitis is common and much is known about its management, further research could lead to targets identified for improvements in care. This study aimed to analyze factors, both medical and socioeconomic, associated with morbidity and mortality at a safety net hospital.

This was a retrospective review of patients with acute pancreatitis admitted between 2015 and 2022. Variables were collected from the electronic medical record and primary outcomes of interest were morbidity and mortality. Standard statistics were used for analysis.

Of the 404 patients that met inclusion criteria, the average age was 48 y, 46% were female, the majority were English speaking, most were Black, and the majority had public insurance. Four percent of patients died and 19.6% had a complication within 30 d. Most patients were admitted to medicine. Public insurance or self-pay status was associated with complications, as was presence of comorbidities and interventional radiology consultation. Surgery and interventional radiology consultation, among other factors, were associated with mortality. Thirty-nine percent of patients with gallstone pancreatitis underwent cholecystectomy. Many patients were started on antibiotics, and of those, 44.1% had no clear indication.

This study reveals novel factors associated with morbidity and mortality in patients with acute pancreatitis, as well as demonstrating that best practices are not uniformly practiced. The study provides further areas of study, including investigations into best pathways for consultations of services and admission service, interventions for at risk patients to improve morbidity and mortality, and how to reduce inappropriate antibiotic use.

Acute pancreatitis in pregnancy is a rare but serious condition that can lead to high maternal mortality and fetal loss. Instances of pregnancy complicated by severe acute pancreatitis, particularly with subsequent respiratory and cardiac arrest, are rarely reported.

We present the case of a 35-year-old woman, at 36 + 5 weeks of gestation, who presented with paroxysmal epigastric pain accompanied by low back pain, nausea, and vomiting. According to the clinical symptoms, B-ultrasound imaging and biochemical indicators, the patient was diagnosed with acute pancreatitis and initially managed conservatively. However, 3 hours after admission, the patient experienced respiratory and cardiac arrest, and the fetus died. In this case, the adverse outcomes occurred due to the lack of aggressive fluid resuscitation and an active surgical intervention.

Implementing aggressive fluid resuscitation to sustain tissue perfusion, alongside the proactive evaluation of pharmacological agents that suppress gastric acid secretion and inhibit pancreatic enzyme activity, may be beneficial in mitigating the risk of a severely adverse prognosis. Effective management of acute pancreatitis during pregnancy requires careful timing of surgical intervention, a thorough evaluation of the risks and benefits regarding the continuation or termination of pregnancy, and a focus on safeguarding both maternal and fetal health.

Macrophage infiltration and activation is a critical step during acute pancreatitis (AP). NLRP3 inflammasomes in macrophages plays a critical role in mediating pancreatic inflammatory responses. Qing-Yi Decoction(QYD)has been used for many years in clinical practice of Nankai Hospital combined with traditional Chinese and western medicine treatment of acute pancreatitis. Although QYD has a well-established clinical efficacy, little is known about its bioactive ingredients, how they interact with different therapeutic targets and the pathways to produce anti-inflammatory effects. Here, we elucidate the therapeutic effects of QYD against acute pancreatitis and reveal its mechanism of action.

The main components of QYD were identified using UHPLC-Q-Orbitrap MS. Network pharmacology was employed to predict potential therapeutic targets and their mechanisms of action. C57BL/6 mice were randomly divided into control group, model group, low, medium and high dose (6, 12, 24 g/kg) QYD groups, with 10 mice in each group. The therapeutic effect of QYD on cerulein-induced acute pancreatitis. (CER-AP) was evaluated by histopathological score, immunohistochemistry, serum amylase and cytokines detection by ELISA. The protein expressions of MyD88/NF-κB/NLRP3 signaling pathway were detected by Western blotting. Along with molecular docking of key bioactive compounds and targets, RAW264.7 cells stimulated with 1μg/ml LPS is used to screen components with more potent effects on target proteins. AR42 J cells were stimulated with 100 nM dexamethasone (dexa) combined with 10 nM cerulein (CN) as s a cell-culture model of acute pancreatitis. Inhibitory effects of the main chemical composition Wogonoside on NLRP3 inflammasomes were analyzed by qRT-PCR and Western blots.

Using UHPLC-Q-Orbitrap MS, 217 compounds were identified from QYD, including Wogonoside, Catechins, Rhein, etc. A visualization network of QYD-compounds-key targets-pathways-AP show that QYD may modulate PI3K-Akt signaling pathway, NOD-like receptor signaling pathway, MAPK signaling pathway, Ras signaling pathway and Apoptosis signaling pathway by targeting TNF, IL1β, AKT1, TP53 and STAT3 exerting a therapeutic effect on AP. QYD administration effectively mitigated CER-induced cytokine storm, pancreas edema and serum amylase. QYD (12 mg/kg) showed better effect. The protein expression levels of MyD88, NF-κB, NLRP3, Caspase-1 and GSDMD in pancreatic tissue were significantly decreased. Through molecular docking and LPS-RAW264.7 inflammation model, the selected Wogonoside significantly decreased IL-1β mRNA. The expression levels of NLRP3/Caspase-1/GSDMD pathway-related proteins were also decreased on AR42J-AP.

The results of network pharmacology indicate that QYD can inhibit AP through multiple pathways and targets. This finding was validated through in vivo tests, which demonstrated that QYD can reduce AP by inhibiting NLRP3 inflammasomes, additionally, it should be noted that 12mg/kg was a relatively superior dose. One of the main chemical compositions Wogonoside regulated NLRP3 inflammasome activation to protect against AP. This study is the first to verify the intrinsic molecular mechanism of QYD in treating AP by combining network pharmacology and animal experiments. The findings can provide evidence for subsequent clinical research and drug development.

Pancreas divisum, resulting from incomplete fusion of the pancreatic ducts during development, disrupts normal drainage and can lead to recurrent acute and chronic pancreatitis. This report presents a case of a 46-year-old male with chronic necrotizing pancreatitis secondary to pancreas divisum. The patient experienced multiple hospital admissions and underwent a cholecystectomy before the underlying etiology, pancreas divisum, was identified after six hospitalizations. This case highlights the diagnostic challenges of recurrent pancreatitis, emphasizing the importance of considering congenital pancreatic anomalies in patients with unexplained or refractory disease. It also underscores the need for a systematic approach to evaluating recurrent pancreatitis to avoid delays in diagnosis and unnecessary interventions. Pancreas divisum is associated with recurrent pancreatitis in a subset of patients. While endoscopic retrograde cholangiopancreatography remains the gold standard for diagnosis and intervention, non-invasive imaging such as magnetic resonance cholangiopancreatography is preferred for initial diagnosis. Endoscopic treatment, including minor papilla papillotomy and stenting, is typically effective for symptomatic cases. However, surgery may be necessary when these methods fail.

Acute on chronic pancreatitis (ACP) shares a similar clinical presentation with acute pancreatitis (AP) and is often diagnosed and treated in the same way. However, these two conditions may have distinct clinical risk profiles and prognoses. There is currently limited evidence available regarding the specific characteristics of ACP.

This retrospective cohort study included all adult patients admitted with a diagnosis of AP or ACP between 2017 and 2019 at two tertiary referral centers. The primary outcome was disease severity as defined by the Atlanta classification. Secondary outcomes included the presence of local and systemic complications, organ failure, ICU admission, and mortality. Differences in outcomes between ACP and AP were compared using multivariate logistic regression models, with results presented as odds ratios (ORs).

We included 1163 patients, 90% of whom had AP and 10% had ACP. ACP patients were predominantly male (81 vs. 46%; P  < 0.001), whereas AP patients were older (mean age 62.6 vs. 56.5 years, P  < 0.001). ACP patients had lower amylase and lipase levels ( P  < 0.001). Multivariate analysis showed no difference in the risk of moderate or severe pancreatitis (OR, 1.15; 95% CI, 0.66-1.98; P  = 0.615). ACP patients had a higher risk of local complications (predominantly pseudocysts) (OR, 1.71; 95% CI, 1.00-2.92; P  = 0.049) and a lower risk of organ failure ( P  = 0.019) and ICU admission ( P  = 0.005).

Our study confirms previous observations that ACP has a more favorable in-hospital prognosis than AP and extends these findings to a modern European setting.

This review addresses oxidative stress and redox signaling in the pancreas under healthy physiological conditions as well as in acute pancreatitis, chronic pancreatitis, pancreatic cancer, and diabetes. Physiological redox homeodynamics is maintained mainly by NRF2/KEAP1, NF-κB, protein tyrosine phosphatases, peroxisome proliferator-activated receptor-γ coactivator 1α (PGC1α), and normal autophagy. Depletion of reduced glutathione (GSH) in the pancreas is a hallmark of acute pancreatitis and is initially accompanied by disulfide stress, which is characterized by protein cysteinylation without increased glutathione oxidation. A cross talk between oxidative stress, MAPKs, and NF-κB amplifies the inflammatory cascade, with PP2A and PGC1α as key redox regulatory nodes. In acute pancreatitis, nitration of cystathionine-β synthase causes blockade of the transsulfuration pathway leading to increased homocysteine levels, whereas p53 triggers necroptosis in the pancreas through downregulation of sulfiredoxin, PGC1α, and peroxiredoxin 3. Chronic pancreatitis exhibits oxidative distress mediated by NADPH oxidase 1 and/or CYP2E1, which promotes cell death, fibrosis, and inflammation. Oxidative stress cooperates with mutant KRAS to initiate and promote pancreatic adenocarcinoma. Mutant KRAS increases mitochondrial reactive oxygen species (ROS), which trigger acinar-to-ductal metaplasia and progression to pancreatic intraepithelial neoplasia (PanIN). ROS are maintained at a sufficient level to promote cell proliferation, while avoiding cell death or senescence through formation of NADPH and GSH and activation of NRF2, HIF-1/2α, and CREB. Redox signaling also plays a fundamental role in differentiation, proliferation, and insulin secretion of β-cells. However, ROS overproduction promotes β-cell dysfunction and apoptosis in type 1 and type 2 diabetes.

Acute pancreatitis is a commonly encountered pathology in the emergency department. We presented a clinical review summarizing the contemporary emergency medicine approach to managing acute pancreatitis. Although the diagnostic criteria for acute pancreatitis are straightforward, it has many possible causes, several treatment options, and both short- and long-term sequelae. We discussed diagnostic, intervention, and disposition considerations relevant to emergency clinicians and considered risk assessment using available clinical decision tools. We also discussed changes to traditional treatments and ongoing investigational therapies, including steroids, monoclonal antibodies, and calcium release-activated calcium channel inhibitors.

Pancreatic diseases, such as acute pancreatitis (AP), chronic pancreatitis (CP), and pancreatic ductal adenocarcinoma (PDAC), disproportionately affect Black/African American (AA) communities in the United States, leading to high incidence, prevalence, and mortality rates. This paper outlines disparities in pancreatic diseases among AAs and explores contributing factors beyond individual biology and behavior, emphasizing the role of social determinants of health (SDoH), including poor access to healthcare, lack of inclusion in research studies, and other crucial systemic and structural factors in historically marginalized AA communities. This review identifies barriers to pancreatic disease research in AAs and advocates for addressing healthcare disparities through community engagement, healthcare workforce diversity, partnerships with minority-serving healthcare facilities, and community-led initiatives targeting lifestyle modification. In conclusion, reducing pancreatic disease disparities in AA communities requires acknowledging systemic influences, engaging frontline communities, implementing innovative healthcare delivery models, addressing modifiable risk factors and structural inequities, and promoting inclusivity in research and healthcare.

Hidradenitis suppurativa (HS) is a chronic, inflammatory and common skin disease. Observation studies have reported the association between HS and cancers, however no studies reported whether a causal relationship exists between HS and cancers. This study aimed to explore the causal relationship between HS and differential subtypes of cancers by conducting a bidirectional Mendelian randomization (MR) analysis.

Genome-wide association study (GWAS) data related to HS and 16 subtypes of cancers were collected. The inverse variance weighted (IVW) method was primarily applied for our MR analysis, MR-Egger, weighted median, simple mode, and weighted mode methods were used additionally. Heterogeneity, horizontal pleiotropy, and potential outliers were assessed for the MR analysis results. Subsequently, disease-related genes were retrieved from the GeneCards database. To investigate the potential functions of these associated genes, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted.

The results of our MR analysis indicated a causal association between HS and pancreatic cancer (PAC). Specifically, HS was found to elevate the risk of developing PAC (odds ratio (OR), 1.074; 95% confidence interval (CI) 1.015-1.135; p = 0.013). Conversely, reverse MR analysis demonstrated that PAC does not exert a causal effect on HS. Furthermore, our findings did not reveal any significant causal relationships between HS and other types of cancer. No evidence of heterogeneity or pleiotropy was identified in the analysis. Additionally, we identified disease-related genes, and subsequent GO and KEGG enrichment analyses indicated that the genes common to both HS and PAC are implicated in pathways associated with immune and inflammatory processes.

The results of this study offer novel evidence regarding the causal relationship between HA and PAC. Our Mendelian randomization analysis indicates that HS may have a causal influence on PAC, which could inform the development of improved treatment strategies for patients suffering from HS. However, the underlying mechanisms warrant further exploration.

Population-based data on the life expectancy and mortality for acute (AP) and chronic pancreatitis (CP) in the United States are limited. This study evaluates the life expectancy, mortality rates and the cause of death in AP and CP patients.

Using the nationwide Veterans Administration database from 1999 to 2015, we identified AP and CP patients (using ICD-9 codes) and non-pancreatitis patients (controls). Age at the time of death was used as a surrogate indicator of life expectancy. Life expectancy in AP and CP patients was compared with the controls, using Cox-proportional hazards model. The mortality rates and cause of death for AP, CP, and controls were also assessed.

Overall, we selected 35,550 AP and 12,545 CP patients and 100,000 controls. The life expectancy was significantly lower for both AP (69 years) and CP (71 years) patients compared to the controls (81 years, p < 0.001). The risk of mortality was higher for AP (adjusted hazard ratio (aHR) 1.61, 95% CI 1.58-1.65, p < 0.001) and CP (aHR 1.64, 95% CI 1.59-1.68, p < 0.001) than in controls. Approximately forty-two percent of all patients died during the follow-up (AP-44.3%, CP-52.1% and controls-39.7%). Circulatory disorders, neoplasms, and respiratory disorders were the leading causes of death in AP and CP patients.

Acute and chronic pancreatitis are associated with decreased life span and higher mortality emphasizing their clinical importance. Although the deaths due to gastrointestinal/digestive system disorders were significantly higher, most of the deaths in AP and CP patients were primarily due to non-gastrointestinal causes.

Alcoholic chronic pancreatitis (ACP) exacerbates pancreatic damage through acinar cell injury, fibroinflammation, and cyclic adenosine monophosphate response element binding protein 1 (CREB) activation, surpassing the damage by alcohol (A) alone or cerulein-induced CP. The molecular cooperativity between CREB and oncogenic Kras G12D/+ (Kras*) in promoting pancreatic cancer progression within the context of ACP remains unclear.

Experimental ACP induction was established in multiple mouse models, with euthanasia during the recovery stage to assess tumor latency. We established CREB deletion (Creb fl/fl ) in Ptf1a CreERTM/+ ;LSL-Kras G12D/+ (KC) genetic mouse models (KCC -/- ). Pancreata from Ptf1a CreERTM/+ , KC, and KCC -/- mice were analyzed using western blotting, phosphokinase array, and quantitative PCR. Single-cell RNA sequencing was performed in ACP-induced KC mice. Lineage tracing of acinar cell explant cultures and analysis of tissue samples from human pancreatic diseases (CP and pancreatic ductal adenocarcinoma [PDAC]) were conducted.

ACP induction in KC mice impaired the pancreas' repair mechanism. Acinar cell-derived ductal lesions demonstrated prolonged hyperactivated CREB in acinar-to-ductal metaplasia (ADM)/pancreatic intraepithelial neoplasia (PanIN) lesions associated with pancreatitis and in PDAC. Persistent CREB activation reprogrammed acinar cells, increasing profibrotic inflammation. In ACP-induced models, acinar-specific Creb ablation reduced advanced PanIN lesions, hindered tumor progression, and improved acinar cell function. Pharmacological targeting of CREB significantly reduced the primary tumor burden in a PDAC mouse model with ACP.

Our findings demonstrate that CREB and Kras* promote irreversible ADM, accelerating pancreatic cancer progression with ACP. Targeting CREB offers a promising strategy to address the clinical need for effective treatments for inflammation-driven pancreatic cancer.

Pancreatitis is a prominent and severe type of inflammatory disorder that has grabbed a lot of scientific and clinical interest to prevent its onset. It should be detected early to avoid the development of serious complications, which occur due to long-term damage to the pancreas. The accurate measurement of biomarkers that are released from the pancreas during inflammation is essential for the detection and early treatment of patients with severe acute and chronic pancreatitis, but this is sub-optimally performed in clinically relevant practices, mainly due to the complexity of the procedure and the cost of the treatment. Clinically available tests for the early detection of pancreatitis are often time-consuming. The early detection of pancreatitis also relates to disorders of the exocrine pancreas, such as cystic fibrosis in the hereditary form and cystic fibrosis-like syndrome in the acquired form of pancreatitis, which are genetic disorders with symptoms that can be correlated with the overexpression of specific markers such as creatinine in biological fluids like urine. In this review, we studied how to develop a minimally invasive system using hydrogel-based biosensors, which are highly absorbent and biocompatible polymers that can respond to specific stimuli such as enzymes, pH, temperature, or the presence of biomarkers. These biosensors are helpful for real-time health monitoring and medical diagnostics since they translate biological reactions into quantifiable data. This paper also sheds light on the possible use of Ayurvedic formulations along with hydrogels as a treatment strategy. These analytical devices can be used to enhance the early detection of severe pancreatitis in real time.

Intraductal papillary mucinous neoplasm (IPMN) can progress into malignant pancreatic cancer, posing challenges in accurately assessing the risk of malignancy. While the nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain containing 3 (NLRP3) inflammasome pathway's role in pancreatic ductal adenocarcinoma (PDAC) has been extensively studied, its implications in IPMN remain unexplored. This study aimed to investigate the prognostic significance of NLRP3 inflammasome-related proteins across IPMN subtypes and their associations with tumor characteristics, with a secondary focus on comparing expression patterns in IPMN and PDAC. A cohort of 187 patients (100 IPMN and 87 PDAC) underwent high-dimensional histopathological imaging using the multiplexed immunohistochemical consecutive staining on single slide method and a semi-automated image analysis workflow. Expression levels of NLRP3, apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC), caspase-1, interleukin-1 beta, interleukin-18 (IL-18), interleukin-1 receptor antagonist, and interleukin-18 binding protein (IL-18BP) were evaluated and compared between IPMN and PDAC samples. The relationships between protein expression and tumor characteristics were examined. Principal component analysis distinguished between intestinal and nonintestinal clusters based on NLRP3-associated proteins. Lower IL-18 expression was linked to the intestinal subtype, while higher caspase-1 was linked to the pancreatobiliary subtype. Elevated caspase-1 and ASC expression were associated with invasiveness in IPMN. No significant correlation was found between the examined proteins and later-stage tumor characteristics in invasive cases. The IL-18/IL-18BP ratio was an independent prognostic factor in invasive IPMN. Our findings highlight the prognostic significance of IL-18 and the IL-18/IL-18BP ratio in invasive IPMNs. These results point to a complex regulation of NLRP3 inflammasome proteins, especially effector cytokines, in pancreatic neoplasms, which are strongly linked to subtype and prognosis.

Recurrent acute pancreatitis (RAP) is a complex syndrome that presents variably, with many cases remaining idiopathic after thorough diagnostics. For evaluating structural etiologies, endoscopic ultrasound and MR cholangiopancreatography are preferred over endoscopic retrograde cholangiopancreatography (ERCP) given their more favorable risk profile and sensitivity. The diagnostic work-up remains paramount since treatment should focus on addressing underlying causes such as early cholecystectomy for gallstone pancreatitis. As more etiologic factors are uncovered, such as genetic susceptibility, causality becomes more nuanced. Earlier enthusiasm for endoscopic sphincterotomy as a treatment for idiopathic RAP has been tempered by less favorable studies in recent years.

Acute pancreatitis (AP) may obscure small pancreatic cancers (PCs) on computed tomography during the acute phase. Surveillance with magnetic resonance cholangiopancreatography (MRCP) and endoscopic ultrasonography (EUS) may enhance early detection and improve patient outcomes. This study evaluated the impact of early MRCP/EUS surveillance on PC outcomes in AP patients and identified high-risk subgroups for early screening.

We retrospectively analyzed 1562 AP patients treated between 2010 and 2021, categorizing them into early surveillance (MRCP/EUS within three months of AP onset; n = 760) and nonearly surveillance groups (n = 802). Key outcomes included time to PC diagnosis, surgical resection rate, tumor stage, and overall survival. Multivariate analysis was performed to identify risk factors for concealed PC in AP patients.

Among 27 PC cases analyzed, the early surveillance group achieved significantly earlier diagnosis, higher surgical resection rates, increased detection of early-stage PC, and improved overall survival compared with the nonearly surveillance group. Multivariate analysis revealed that subthreshold main pancreatic duct (MPD) dilation (≥2.5 mm) and moderately severe AP were significant predictors of PC.

Early MRCP/EUS surveillance in AP patients facilitates timely detection of occult PC and enhances patient prognosis. These findings support prioritizing early surveillance for AP patients with subthreshold MPD dilation and moderately severe disease. Further large-scale studies are warranted to validate these strategies in clinical practice.

Triglyceride-Glucose (TyG) index, a novel surrogate marker for insulin resistance, has been linked to the risk of various cancers, such as breast and colorectal cancers. However, the relationship between the TyG index and its related indices with the risk of pancreatic cancer(PC) remains unclear.

This large-scale, prospective cohort study utilized data from the UK Biobank, involving 428,152 participants who were free of PC at baseline. The primary outcome was incident PC. To evaluate the relationships between TyG-related indices and PC onset, covariate-adjusted Cox proportional hazards regression models and restricted cubic spline (RCS) analyses were employed. Additionally, we explored the relationships between TyG-related indices and incident PC within subgroups defined by age, gender, diabetes, hypertension, pancreatitis history, smoking status, and drinking status. Sensitivity analyses were conducted to confirm the robustness of our findings.

Over an average follow-up period of 13.8 years, a total of 1,759 PC cases occurred. The risk of developing PC increased with higher levels of TyG-related indices. RCS curves illustrated a linear positive relationship between TyG-related indices and incident PC. Subgroup analyses indicated that the relationships between the TyG index, TyG-waist circumference, and TyG-waist-to-hip ratio and PC risk were more pronounced in participants without hypertension, without pancreatitis history, and those with drinking history (P for interaction < 0.05). Sensitivity analyses further validated the robustness of these findings.

TyG-related indices were independently related with a higher risk of incident PC, highlighting the importance of incorporating these indices into PC risk assessment tools and provides strong support for constructing a more comprehensive PC risk assessment framework.

Acute pancreatitis (AP) is characterised by self-digestion of the pancreas by its own proteases. This pathophysiological initiating event in AP occurs inside pancreatic acinar cells where intrapancreatic trypsinogen becomes prematurely activated by cathepsin B (CTSB), and induces the digestive protease cascade, while cathepsin L (CTSL) degrades trypsin and trypsinogen and therefore prevents the development of AP. These proteases are located in the secretory compartment of acinar cells together with cystatin C (CST3), an endogenous inhibitor of CTSB and CTSL. The results are based on detailed biochemical analysis, site-directed mutagenesis and molecular dynamics simulations in combination with an experimental disease model of AP using CST3 deficient mice. This identifies that CST3 is a critical regulator of CTSB and CTSL activity during AP. CST3 deficient mice show a higher intracellular CTSB activity resulting in elevated trypsinogen activation accompanied by an increased disease severity. This reveals that CST3 can be cleaved by trypsin disabling the inhibition of CTSB, but not of CTSL. Furthermore, dimerised CST3 enhances the CTSB activity by binding to an allosteric pocket specific to the CTSB structure. CST3 shifts from an inhibitor to an activator of CTSB and therefore fuels the intrapancreatic protease cascade during the onset of AP.

Acute pancreatitis (AP) is an acute inflammatory disease resulting from abnormal digestion of itself and surrounding organs by pancreatic enzymes caused by a variety of pathogenic factors. When the tissue of a biological organism is afflicted with pancreatitis and experiences swelling, bleeding, and necrotic injuries, the abnormal expression of β-galactosidase (β-Gal) activity becomes one of the main indicators for assisting in the diagnosis of pancreatitis. In this study, a highly specific red fluorescent probe designed for the detection of β-Gal activity has been developed. β-galactoside is used as the enzyme activating group, and the long-wavelength luminescent water-soluble organic molecule NBDOH is used as the luminophore to construct the fluorescent probe NBD-gal. NBD-gal is activated by abnormally overexpressed β-Gal, releasing a strong red fluorescent signal. The new fluorescent probe developed in this study is used to assist in the diagnosis of pancreatitis by detecting abnormal expression of β-Gal activity in vivo. In in vivo imaging experiments, NBD-gal can effectively differentiate between normal nude mice and pancreatitis nude mice. In addition, NBD-gal can be effectively localized in real-time to the pancreas and intestines, which are rich in β-Gal in nude mice. Therefore, NBD-gal exerts great potential in the early diagnosis, treatment, and prevention of biomedical clinical pancreatitis.

Severe acute pancreatitis (SAP) leads to systemic inflammation, resulting in multiorgan damage. Acute lung injury and acute respiratory distress syndrome develop in one-third of SAP patients, with a high mortality rate of 60% due to secondary complications. Patients with pancreatitis often have selenium deficiency, and selenium supplements may provide beneficial effects. This study examined the protective role of selenium in a model of SAP induced by caerulein + lipopolysaccharide (cae + LPS). Mice were administered selenium (1 mg/kg) before being challenged with caerulein (6 injections of 50 μg/kg) and LPS (10 mg/kg). At 3 h after the last caerulein injection, blood was collected for estimating pancreatic enzymes and cytokine levels, and the mice were euthanized. We performed morphological and histological studies, measured levels of protease and oxidative stress markers and conducted western blot, ELISA, and RT-qPCR analyses. We examined lung tissue histologically and estimated myeloperoxidase levels. Selenium pretreatment significantly reduced pancreatic enzyme levels such as amylase, lipase, and proteases (specifically MMPs) and reversed tissue injury in the pancreas and lungs caused by cae + LPS. In addition, selenium-treated mice showed decreased levels of inflammatory markers and chemokines. Examination of the downstream inflammatory pathways confirmed the protective effect of selenium, which mediates its anti-inflammatory and antioxidant action by inhibiting the major inflammatory signaling pathways (MAPKs, NF-κB, and STAT3) and activating the phosphorylation of Nrf2 via Nrf2/HO-1 pathways. These findings suggest that selenium may be a potential therapeutic option for treating SAP-associated secondary complications.

Increased systemic concentrations of YKL-40 are seen in various inflammatory conditions. We explored the relationship between the serum YKL-40 concentrations and subsequent disease severity in patients with acute pancreatitis (AP).

Consecutive adults with AP were prospectively enrolled, and classified as having mild, moderate or severe disease. On admission and 48 h later, C-reactive protein (CRP), YKL-40, interleukin-6 and 8 (IL-6, IL-8), and tumor necrosis factor alpha (TNF-α) concentrations were measured. Patients were also classified as those with low (<50 ng/mL, in the range seen in 30 age and sex-matched non-AP subjects), high (≥190 ng/mL, seen in most of the other inflammatory conditions), and intermediate YKL-40 (50-189 ng/mL).

Incidence of mild, moderate and severe AP among the 150 enrolled patients was 80 (53.3 %), 59 (39.3 %), and 11 (7.4 %), respectively. Both on admission and 48 h later, high YKL-40 (vs. intermediate or low) was strongly associated with higher odds of a more severe AP, independently of the concurrent IL-8 and TNF-α concentrations (OR around 3.5-4.0, or higher). On admission, the association was independent also of the concurrent CRP, whereas the association between the later concentrations and the outcome was conditional on CRP - uncertain at low, strong at high CRP. The high YKL-40 - outcome association at both time-points was conditional on concurrent IL-6: uncertain if IL-6 was low, strong if IL-6 was high.

Serum YKL-40 is a plausible candidate for further evaluation as an early biochemical indicator of subsequent AP severity, particularly if considered jointly with CRP and/or IL-6.

The IL-2 family, consisting of IL-2, IL-4, IL-7, IL-9, IL-15 and IL-21, is a key regulator of the immune response. As an important endocrine and digestive organ, the function of the pancreas is regulated by the immune system. Studies have shown that each cytokine of the IL-2 family influences the occurrence and development of pancreatic diseases by participating in the regulation of the immune system. In this paper, we review the structural and functional characteristics of IL-2 family members, focus on their molecular mechanisms in pancreatic diseases including acute pancreatitis, chronic pancreatitis and pancreatic cancer, and highlight the importance of the related proteins in the regulation of immune response and disease progression, which will provide valuable insights for new biomarkers in pancreatic diseases, early diagnosis of the diseases, assessment of the disease severity, and development of new therapeutic regimens. The insights of the study are summarized in the following sections.

Groove pancreatitis (GP) is a chronic segmental pancreatitis which leads to altered pancreatic secretions and pancreatitis. The exact pathogenesis of GP has not been clearly identified to date but heavy smoking and chronic alcohol consumption seem to be the main factors involved. The resulting chronic pancreatitis (CP) is a debilitating disease causing abdominal pain often refractory to medical therapy, so much that the main indication for surgical treatment is intractable abdominal pain. A growing number of increasingly complex and diverse surgical operations for the treatment of this disease were reported. Operative procedures for CP are currently grouped into decompression procedures and pancreatic resections. No consensus about which one leads to the best outcomes, but every case should be tailored to specific clinical scenarios and single individuals. We report the case of a 44-year-old man with intractable abdominal pain due to GP underwent to Partington-Rochelle modified procedure. A Wirsung-jejunal side-to-side anastomosis as described by Partington-Rochelle was performed but with two variations: the first was the length of the anastomosis which was < 50 mm (short anastomosis), while the second was the placement of two removable Bracci stent tube 6 Fr to drain respectively the distal and the proximal-medium part of Wirsung duct. The post-operative course was uneventful with good pain control. During follow-up no evidence of any radiologic signs of infection or fluid collections or pancreatic fistula nor recrudescent of abdominal pain. Nowadays a uniform approach to this pathology still is lacking. Although surgery can be carried out with satisfactory results in specialized centers, the specifical operation type should be tailored to every single cases.

Acute pancreatitis (AP) is a disease characterized by an acute inflammatory response in the pancreas. This is caused by the abnormal activation of pancreatic enzymes by a variety of etiologic factors, which results in a localized inflammatory response. The symptoms of this disease include abdominal pain, nausea and vomiting and fever. These symptoms are induced by a hyperinflammatory response and oxidative stress. In recent years, research has focused on developing anti-inflammatory and antioxidative therapies for the treatment of acute pancreatitis (AP). However, there are still limitations to this approach, including poor drug stability, low bioavailability and a short half-life. The advent of nanotechnology has opened up a novel avenue for the management of acute pancreatitis (AP). Nanomaterials can serve as an efficacious vehicle for conventional pharmaceuticals, enhancing their targeting ability, improving bioavailability and prolonging their half-life. Moreover, they can also exert a direct therapeutic effect. This review begins by introducing the general situation of acute pancreatitis (AP). It then discusses the pathogenesis of acute pancreatitis (AP) and the current status of treatment. Finally, it considers the literature related to the treatment of acute pancreatitis (AP) by nanomaterials. The objective of this study is to provide a comprehensive review of the existing literature on the use of nanomaterials in the treatment of acute pancreatitis (AP). In particular, the changes in inflammatory markers and therapeutic outcomes following the administration of nanomaterials are examined. This is done with the intention of offering insights that can inform subsequent research and facilitate the clinical application of nanomaterials in the management of acute pancreatitis (AP).

Acute pancreatitis is an inflammatory condition of the exocrine pancreas that is a common indication for hospital admission and has had an increasing incidence in the last few decades. The diagnosis of acute pancreatitis requires the satisfaction of two out of three criteria: (1) abdominal pain radiating to the back, (2) serum lipase or amylase levels three or more times the upper limit of the normal level, and (3) findings indicating pancreatitis obtained via a computed tomography (CT) scan or magnetic resonance imaging (MRI). The different etiologies include gallstones, autoimmune disorders, alcohol abuse, smoking, hypertriglyceridemia, obesity, drugs, and post-endoscope retrograde cholangiopancreatography (ERCP). The initial investigation includes serum amylase and lipase analysis, a lipid panel including triglycerides, analysis of immunoglobulins, a full blood count, electrolyte analysis, a hemoglobin A1c test, a complete metabolic panel, and transabdominal ultrasound. The initial therapy includes oxygen supplementation, the provision of intravenous fluids, pain control, and a nutrition regime. Early oral feeding is encouraged if tolerated; if not, liquid supplement provision or enteral tube feeding within 48 h of admission has shown better outcomes. Some complications of acute pancreatitis are necrosis, infection, insulin resistance leading to diabetes mellitus, and pancreatic exocrine insufficiency requiring enzyme supplementation. Patients need to attend regular follow-ups and abstain from alcohol and smoking (if warranted) to prevent the recurrence of acute pancreatitis. The mortality rate of acute pancreatitis has decreased in the past few decades because of better management skills, but the recent rise in acute pancreatitis episodes is concerning. Sustained endeavors through clinical trials are required to establish a broad variety of drugs that can be used for acute pancreatitis episodes.